The objective of this study is to investigate the mechanisms of several biochemical endocrinopathies we have observed in obesity. 1) Urinary excretion of radioactivity from 3H-estradiol is inversely proportional to fat weight in obese women but is constant regardless of fat weight in obese men; this is hypothesized to be due to a sex difference in estrogen receptors in adipose tissue and these receptors will be quantitated in vitro. 2) 24-Hour mean plasma cortisol concentration varies inversely with fat weight in obese women but is constant regardless of fat weight in obese men; this is hypothesized to be due to a sex difference in corticosteroid receptors in adipose tissue and these receptors will be quantitated in vitro. 3) Plasma estrogen levels are elevated in obese men and women, but the elevation is predominantly of estrone in men and of estradiol in women; this is hypothesized to be due to a sex difference in the set-point of the E2 yields reversibly E1 equilibrium, which will be measured by administration of (4-14C, 17-3H)-estradiol and suitable kinetic studies. 4) Plasma FSH levels and sperm production are subnormal in obese men. The apparent hypogonadotropic hypogonadism in these men is hypothesized to be due to their elevated estrogen levels; this hypothesis will be tested by giving corticosteroids to suppress the source of the increased estrogen (i.e. adrenocortical androstenedione) to see whether this will normalize plasma estrogen and FSH levels.